Distinctive aspects of peptic ulcer disease, Dieulafoy's lesion, and Mallory-Weiss syndrome in patients with advanced alcoholic liver disease or cirrhosis

Abstract

Aim: To systematically review the data on distinctive aspects of peptic ulcer disease (PUD), Dieulafoy's lesion (DL), and Mallory-Weiss syndrome (MWS) in patients with advanced alcoholic liver disease (aALD), including alcoholic hepatitis or alcoholic cirrhosis.

Methods: Computerized literature search performed via PubMed using the following medical subject heading terms and keywords: "alcoholic liver disease", "alcoholic hepatitis"," alcoholic cirrhosis", "cirrhosis", "liver disease", "upper gastrointestinal bleeding", "non-variceal upper gastrointestinal bleeding", "PUD", ''DL'', ''Mallory-Weiss tear", and "MWS''.

Results: While the majority of acute gastrointestinal (GI) bleeding with aALD is related to portal hypertension, about 30%-40% of acute GI bleeding in patients with aALD is unrelated to portal hypertension. Such bleeding constitutes an important complication of aALD because of its frequency, severity, and associated mortality. Patients with cirrhosis have a markedly increased risk of PUD, which further increases with the progression of cirrhosis. Patients with cirrhosis or aALD and peptic ulcer bleeding (PUB) have worse clinical outcomes than other patients with PUB, including uncontrolled bleeding, rebleeding, and mortality. Alcohol consumption, nonsteroidal anti-inflammatory drug use, and portal hypertension may have a pathogenic role in the development of PUD in patients with aALD. Limited data suggest that Helicobacter pylori does not play a significant role in the pathogenesis of PUD in most cirrhotic patients. The frequency of bleeding from DL appears to be increased in patients with aALD. DL may be associated with an especially high mortality in these patients. MWS is strongly associated with heavy alcohol consumption from binge drinking or chronic alcoholism, and is associated with aALD. Patients with aALD have more severe MWS bleeding and are more likely to rebleed when compared to non-cirrhotics. Pre-endoscopic management of acute GI bleeding in patients with aALD unrelated to portal hypertension is similar to the management of aALD patients with GI bleeding from portal hypertension, because clinical distinction before endoscopy is difficult. Most patients require intensive care unit admission and attention to avoid over-transfusion, to correct electrolyte abnormalities and coagulopathies, and to administer antibiotic prophylaxis. Alcoholics should receive thiamine and be closely monitored for symptoms of alcohol withdrawal. Prompt endoscopy, after initial resuscitation, is essential to diagnose and appropriately treat these patients. Generally, the same endoscopic hemostatic techniques are used in patients bleeding from PUD, DL, or MWS in patients with aALD as in the general population.

Conclusion: Nonvariceal upper GI bleeding in patients with aALD has clinically important differences from that in the general population without aALD, including: more frequent and more severe bleeding from PUD, DL, or MWS.

Keywords: Alcoholic hepatitis; Alcoholic liver disease; Cirrhosis; Dieulafoy lesion; Endoscopic therapy; Mallory-Weiss syndrome; Peptic ulcer disease; Portal hypertension.

Figure 1

Reported distribution of common etiologies of upper gastrointestinal bleeding in patients with cirrhosis. Frequency distribution of the etiologies of upper gastrointestinal bleeding in patients with cirrhosis. Varices include esophageal or gastric varices. Adapted from Ref. [39,44-47]. PUD: Peptic ulcer disease; PHG: Portal hypertensive gastropathy; MWS: Mallory-Weiss syndrome; Other: Other etiologies of upper gastrointestinal bleeding.

Figure 2

Seventy-year-old male with Child-Pugh class A alcoholic cirrhosis presented with hematemesis, melena, and orthostatic dizziness. Esophagogastroduodenoscopy (EGD) revealed an acute 14 mm × 5 mm ulcer in the distal duodenal bulb with stigma of recent hemorrhage (SRH) represented by a prominent, nonbleeding, flat, pigmented spot; trace esophageal varies with no SRH, such as wale bites; and no portal hypertensive gastropathy. Note the deep erosion adjacent to the ulcer. The etiology of the ulcer was idiopathic. The patient had no history of taking nonsteroidal anti-inflammatory drugs or aspirin. Pathologic examination of gastric biopsies taken at EGD revealed no Helicobacter pylori. No endoscopic therapy was performed because the only SRH was a flat pigmented spot which has a low risk of rebleeding. The patient, however, required transfusion of 4 units of packed erythrocytes. The patient was treated medically with pantoprazole with no recurrence of the bleeding. This patient illustrates that peptic ulcers are in the differential of acute upper gastrointestinal bleeding in a patient with cirrhosis, even in the absence of risk factor for peptic ulcers, and that bleeding from peptic ulcers in cirrhotic patients may be unusually severe.